Symposium on Common Orthopedic Problems
Bow Legs and Knock Knees William McDade, M.D. *
Bow legs (genu varum) and knock knees (genu valgum) are common findings that affect the lower extremities of growing children. While the great majority of these problems represent normal physiologic development, and correct themselves in time without treatment, it is important for the physician to differentiate between physiologic angular deformities and those that may be pathologic, requiring special evaluation and treatment. A detailed classification of bow legs and knock knees has been set forth by Stelling and Meyer.27 The most common causes of bow legs and knock knees-physiologic varus and valgus, Blount's disease, rickets, and trauma-are discussed.
Natural History Many authors have attempted to define the natural variation and growth of the lower extremities as they relate to the position of the knee. Bohm5 was the first to suggest that bow legs and knock knees might represent normal growth patterns in infants and children. He described differences in the height and breadth of the proximal tibia and distal femoral epiphysis, suggesting that these variations were a cause for bow legs seen in infancy and knock knees recognized later in childhood. Since that time, others7, 10, 18,20,22 have examined large numbers of children both clinically and radiographically for bow leg and knock knee deformity. Their conclusions are similar and consistent with the recognition of a varoid stage of development of the knees up to the age of two years, which undergoes transition into a valgoid stage of knee development up to about age seven years. These changes are felt to represent normal physiologic development. Extremes of varus and valgus in infancy and childhood are to be expected, and may be related to or accentuated by sleeping positions, posture, ligament laxity, and torsional malalignment. Salenius,20 in the most detailed study to date, examined 1480 infants and children clinically and by x-ray, with computer analysis, using the tibiofemoral angle as a measurement point. Varus was present in in"Assistant Clinical Professor of Orthopaedic Surgery, University of California, San Diego, California Pediatric Clinics of North America- VoL 24, No.4, November 1977
825
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WILLIAM McDADE DEVELOPMENT OF THE TIBIO-FEMORAL ANGLE DURING GROWTH VARUS VALGUS
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Figure 1. Development of the tibiofemoral angle during growth based on 1480 measurements of the tibiofemoral angle of children at different ages. (From Salenius, P.", and Vankka, E.: Development of the tibiofemoral angle in children. J. Bone Joint Surg., 57A:259-261, 1975, with permission.)
Figure 2. A, Leg alignment in this 15 month old boy appears "normal" without evidence of varus or valgus. B, Standing x-ray film of the same infant. The tibiofemoral angle approaches zero. The· epiphyses are ovoid and the transverse planes of the epiphyseal lines of the knee and ankle are relatively horizontal.
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827
fants less than one year of age. The knees began to straighten between the ages of one to one and a half years, and during the second and third year of life the tibiofemoral angle changed to marked valgus, which appeared to correct itself to lesser valgus in later childhood. The tibiofemoral angles were the same in boys and girls (Fig. 1).
"The Normal Infant" The normal infant usually stands with the legs somewhat apart. Infant fat may mask early physiologic varus. Standing x-rays reveal the femur and tibia to be normally aligned, without evidence of significant varus or valgus. There is no significant flaring of the distal femoral and proximal tibial metaphysis, and no asymmetrical cortical thickening of the tibial shaft. The epiphyses are oval, and the transverse planes of the epiphyseal lines are horizontal. The findings are symmetrical (Fig. 2). PHYSIOLOGIC VARUS. A mild degree of bow legs is not uncommon in children under the age of two years. Internal tibial torsion often accompanies physiologic genu varum, and its presence will accentuate the bow leg attitude in stance and with ambulation. X-rays reveal a slight lateral bow of the femur and tibia, giving rise to a varus appearance of the knee. There is flaring of the distal femoral and proximal tibial metaphysis. Thickening of the medial cortical wall of the tibia is commonly seen. The epiphysis may appear wedged medially. The transverse plane of the distal tibial epiphysis is tilted medially. The findings are symmetrical. Physiologic varus should correct by the age of two years (Fig. 3). PHYSIOLOGIC VALGUS. Physiologic knock knee is usually observed at age two and a half or three years. The x-ray appearance of the valgus knee is different, due to the older age of the child with advancing ossification of the skeletal system. The epiphyseal centers are larger, and the metaphyseal ossification has progressed to eliminate much of the metaphyseal flaring. There is no tibial cortical thickening. The planes of the epiphysis are relatively horizontal (Fig. 4). Pes planus and external tibial torsion may accompany genu valgum, and will accentuate the appearance of knock knees (Fig. 5). CLINICAL EVALUATION. Evaluation of the child with varus or valgus deformity should include a family history, leg measurements for inequality and asymmetry, observations for ligament laxity and pes planus, and observations for malalignment of the lower extremities (femoral and tibial torsion). TREATMENT. Recognizing that infants up to the age of one to one and a half years demonstrate a normal physiologic varus, and children between the ages of two and seven years demonstrate a normal physiologic valgus, treatment is not indicated. While sleeping splints, corrective shoes, and active and passive exercises have been advocated, no difference or change in the appearance of the extremities has been noted that would otherwise be expected through normal growth and development. In fact, utilization of the Denis-Browne bar to correct a physiologic genu varum is probably contraindicated, and will only "exaggerate" the physiologic knock knees that will develop later. While shoe correction in the form of wedges may improve the "tracking" with ambula-
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WILLIAM McDADE
Figure 3. A, Twelve month old girl with physiological varus. Note wide-based stance, bow legs, and internal rotation attitude. The lateral flare or prominence of the lower leg is accentuated by the infant fat and internal tibial torsion. B, Standing x-ray. Note the medial flaring of the distal femoral and proximal tibial metaphysis, asymmetrical cortical thickening of the tibia, and the medially directed distal tibial epiphysis. The tibiofemoral angle measures 12° of varus. C, Resolution of physiologic varus at 21 months of age. Note straighter appearance of legs with less toeing in. No treatment was given. D, Standing x-ray. There is less flaring of the femoral and tibial metaphysis. The plane of the distal tibial epiphysis is less medially directed. The tibiofemoral angle measures 3° of varus.
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829
Figure 4. A, Three and one half year old girl with physiological valgus. B, Standing x-ray. Tibiofemoral angle measures 10 0 of valgus. C, Same girl at age eight years. Note clinical improvement in leg alignment without treatment. D, Standing x-ray. Tibiofemoral angle measures 4 0 of valgus.
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WILLIAM McDADE
Figure 5. A. Five year old boy with knock knees and outward rotation of lower legs, and flat feet. B, Examination showing clinical external tibial torsion. External tibial torsion and pes planus will accentuate the appearance of physiologic valgus. C, Standing xrays. Tibiofemoral angle measures 10 of valgus. Despite the similar tibiofemoral angle here and in Figure 4B, note how the external tibial torsion in Figure 5A accentuates the knock knee deformity as compared with Figure 4A (no external tibial torsion). 0
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tion, it will have no effect on the resolution of the normal physiologic varus or valgus. Reassurance and regular follow-up are the only specific treatment indicated for physiologic genu varum or val gum. X-rays are generally not indicated for this group.
Extreme Variation When does normal physiologic bow leg and knock knee represent an "extreme variation" that requires additional evaluation and treatment, and when is it pathologic? Bow legs that are unilateral or asymmetrical and are present beyond the age of two years, particularly in Black infants, may represent pathological conditions that require further investigation. A varus deformity that is not resolving by 18 to 24 months of age with a tibiofemoral angle of 25° or more of varus (on x-ray), especially in a Black infant, has a bad prognosis for spontaneous resolution and should be braced (Figs. 6 and 7). Knock knees in children under the age of seven may be safely ignored, unless excessive (a measured tibiofemoral angle of greater than 15° of valgus), asymmetrical, or accompanied by shortened stature. Howarth l l felt that if a knock knee deformity was excessive (greater than three inches measured between the medial malleoli) at the age of 10 years, the deformity was not likely to correct with time. He believed excessive genu valgum contributed to awkwardness of gait, subluxing patella, easy fatigability, and jOint pains. For this set of circumstances, he recommended surgical stapling of the medial distal femoral and/or medial proximal tibial epiphysis in girls at age 10 or 11 years and boys at age 12 or 13 years to correct the angular deformity. Unilateral or asymmetrical varus or valgus may be associated with tumors, congenital deformities, and trauma, while symmetrical extreme varus or valgus may be a manifestation of metabolic or endocrine disease. Blount's Disease (Tibia Vara) Blount's disease (tibia vara, osteochondrosis deformans tibiae) is a growth distrubance involving the epiphyseal-metaphyseal region of the posterior-medial aspect of the proximal tibia, resulting in a severe bow leg deformity. Significant internal tibial torsion is usually associated with the deformity. The condition was first described by Erlacher in 1922, reviewed and put into proper perspective by Blount in 1937. 3 Two stages of the deformity are recognized: an infantile form which is usually bilateral, progressive, and associated with significant internal tibial torsion; and a juvenile form recognized between the ages of 6 and 14 years which is usually unilateral. The varus deformity is milder but there may be more shortening of the involved leg. The juvenile type is much less common than the infantile type. It is impossible to distinguish between the initial stage of Blount's disease and cases of extreme physiologic genu varum, and it may be that the "extreme variation" of physiologic genu varum represents the initial stage of Blount's disease. The clinical diagnosis is usually not made until the child begins to walk. There appears to be a genetic-famil-
832
Figure 6.
WILLIAM
McDADE
A, The "extreme variation," a 15 month old boy who walked at age 10 months.
B, Internal tibial torsion is present and accentuates the bow leg appearance. C, Standing x-ray. Findings are similar to Figure 3B, but with more metaphyseal flaring, medial wedging of the epiphysis, and more pronounced varus. The tibiofemoral angle measures 25". D, Stand-
ing x-ray at age 21 months. Tibiofemoral angle measures 32" of varus. Normally the physiologic varus should be spontaneously correcting by this age. This degree of deformity represents an "extreme variation" of physiologic varus, is unlikely to improve spontaneously, and may represent the precursor of true Blount's disease. The extreme degree of varus at this age and the poor prognosis in the black infant require treatment with braces at this age. The clinical appearance at this age of extreme physiologic varus cannot be differentiated from the early stage of Blount's disease.
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A
Figure 7. Braces used for treatment of "extreme varus" and Blount's disease: long leg brace with lateral pull strap (A), A-frame brace (B), and Blount brace (C). (Courtesy of Robert Hensinger, M.D., University of Michigan.)
c ial background and geographical distribution, with most cases reported from the West Indies, West Africa, and Scandinavia. Blacks appear to be particularly affected. There is disagreement as to the etiology. LangenskiOld14 , 15 and Blount3 ,4 think the condition represents a disturbance in growth and ossification (dysplasia of bone) of the medial part of the proximal tibial epiphysis-metaphysis, whereas Golding-McNeil,9 Kessel,I3 and Bateson!' 2 believe that. the problem develops as a result of early walking patterns (particularly in Blacks) with abnormal lines of force transmitted across the medial tibiofemoral compartment. RADIOGRAPHIC FINDINGS. Langenskiold14,15 described six stages of x-ray progression (Stages I to VI) of Blount's disease (Fig. 8) based on the degree of epiphyseal depression and metaphyseal fragmentation in-
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WILLIAM McDADE II
III
IV
2-3 years
V
VI
10·13 years
Complete restoration
Restoration
common
possible
Figure 8. X-ray tracings illustrating the various stages of Blount's disease (From LangenskiOld, A.: Tibia vara. Acta Chir. Scand., 103:1-22,1952, with permission.)
volving the proximal medial tibial epiphyseal-metaphyseal junction. The earliest x-ray finding is that of an abrupt medial angulation and fragmentation at the proximal aspect of the tibia (Fig. 9). Stage I may be difficult to distinguis~from the x-ray findings of extreme physiologic genu varum. The progres'sive x-ray findings parallel the progressive clinical deformity in infantile tibia vara. X-ray findings of adolescent tibia vara reveal a lesser degree of varus deformity. The epiphyseal line medially is significantly narrowed (Fig. 10). NATURAL HISTORY OF TREATMENT. Treatment depends upon the degree of deformity (clinical and x-ray) and the age of the patient. The first four years of life are the main period of progression of Blount's disease, after which time the deformity, while continuing to progress, does so at a slower speed. Conservative treatment is recommended under the age of three years with close observation and/or appropriate bracing (see Fig. 7). If the varus deformity is not improving by age 18 months to 2 years, Stages I and II may be braced successfully. For the child who demonstrates a persistent varus with the tibiofemoral angle measuring more than 15 of varus, and Stage III or more, osteotomy is usually required. Bracing may be effective up to the age of three years; but with progressive clinical and x-ray deformity, early osteotomy is recommended (usually between the ages of four and eight years). Osteotomy done at an early age will usually completely correct the deformity permanently, with greater chances for recurrence if the osteotomy is done in later years. 0
Rickets Rickets is a disease process of the growing skeleton caused by a disturbance in calcium and phosphorus metabolism, characterized by inadequate calcification of the bone matrix. Due to the fact that the epiphyseal ends of the bone are the sites of the most active osteogenesis, the disease is most apparent here. Causes of rickets include vitamin D deficiency, renal tubular insufficiency, chronic renal insufficiency, hypophosphatasia, and vitamin D refractoriness. Vitamin D-deficient rickets
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is rarely seen in the United States. Rickets due to renal tubular insufficiency (failure of reabsorption of phosphate) includes many different forms and is becoming more commonly diagnosed. Chronic renal insuffiCiency caused by generalized kidney failure affecting both the glomeruli and tubules (renal rickets, renal osteodystrophy) has become more important with the advent of kidney transplantation and renal dialysis. Hypophosphatasia is an inborn error of metabolism characterized by low alkaline phosphatase activity. Vitamin D-refractory rickets is an inherited disorder treated by the administration of large doses of vitamin D. Figure 9.
Figure 10. Figure 9. X-ray of two year old boy with unilateral Blount's disease (stage I). Figure 10. X-ray of adolescent child with unilateral Blount's disease (stage V).
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WILLIAM McDADE
Figure 11. X-ray appearance of rickets. Note bowing of the legs, widening of the epiphyseal line, and irregularity of the metaphyseal epiphyseal junction.
The clinical picture and x-ray findings in most forms of rickets reveal an individual who may be short in stature with poor muscle tone, joint pain, and with various angular deformities affecting the weight bearing portions of the skeleton, particularly bow legs and knock knees. Genu valgum appears to be particularly common with chronic renal insufficiency, with genu varum being more common in vitamin Ddeficient rickets and vitamin D-refractory rickets. The x-ray findings are relatively similar, with osteoporosis, bowing of the long bones, widening of the epiphyseal plate, fraying of the metaphysis, and cortical thinning (Fig. 11). The diagnosis of the various forms of rickets is made by history, appropriate laboratory studies, and x-ray evaluation. TREATMENT. Recognition of the various forms of rickets and the application of specific treatment programs, plus the advent of renal transplantation and kidney dialysis, have changed the outlook for the ,.child with rickets rather abruptly over the past few years. With proper medical management, a longer life can be expected and a more aggressive approach to the angular deformities affecting these children is reasonable. Treatment of the angular deformity which was often conservative in the past due to the limited lifespan can now be more aggressive to include osteotomies when angular deformities require them. It is recommended that orthopedic care be limited to conservative treatment
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Figure 12. A, X-ray of two year old girl with undisplaced fracture of the proximal tibia. Fibula is not fractured. B, One year later the same girl exhibits pronounced unilateral valgus of previously injured leg. C, Standing x-ray shows valgus of healed tibia. Bowing occurs at the fracture site from tibial overgrowth and tethering effect of uninjured fibula. D, Correction by osteotomy of tibia and fibula. E, Clinical appearance at age five years (two years after osteotomy of tibia and fibula).
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WILLIAM McDADE
until the child is optimally controlled medically. Splints and braces may be used to control angular deformity at this age. No specific guidelines are available for the degree of deformity in rickets requiring osteotomy. Clinical judgment must include the age and maturity of the patient, degree and progression of deformity, and medical status. It is important to remember that four to six weeks prior to any operative procedure vitamin D (if being used) should be discontinued to prevent hypercalcemia and hypercalcinuria with associated kidney and central nervous system damage. Immobilization should be kept at a minimum to prevent osteoporosis. Trauma Trauma to the proximal tibia may take the form of fracture, infection, or surgery. Direct injury to the epiphyseal-metaphyseal complex (particularly the Salter IV and V injuries):!1 may lead to predictable angular deformity. It is not generally recognized that seemingly innocuous injuries of the tibia (undisplaced fractures of the proximal tibial shaft without fracture of the fibula) may lead to progressive valgus of the knee with angulation occurring at the fracture site. 12 , 28 Parents should be advised of this potential deformity (Fig. 12). It has been recognized that asymmetrical valgus may occur from such conditions as osteomyelitis involving the proximal tibia metaphysis, and from surgery performed on the proximal tibia (i.e., osteotomy of the tibia without osteotomy of the fibula). Deformities occur due to stimulation of the proximal tibial growth plate, with a tethering effect rendered by the intact fibula, and development of progressive valguS. 28 Tibial Osteotomy It is not the purpose of this paper to discuss the surgical approach or technique of tibial osteotomy for the correction of genu varum or val gum. However, recent reports l7 , 23, 26 have all documented significant complications in regard to the neurovascular status of the lower extremity in association with osteotomies done on the proximal tibia for rotational or angular deformity. It should be kept in mind that any child who undergoes a tibial osteotomy presents a potential hazard, and should be observed carefully for problems of compromise to the neurovascular or motor status of the lower extremity in the postoperative period. Other Causes of Knock Knees and Bow Legs Many other conditions may cause bow legs and knock knees in children, such as congenital anomalies, tumors, infection, paralytic deformities, metabolic/endocrine disorders, and dysplasias of bone. These conditions each require individual evaluation and treatment. REFERENCES 1. Bateson, E. M.: Non-rachitic bow leg and knock knee deformities in young Jamaican children. Brit. J. Radiol., 39:92-101, 1966. 2. Bateson, E. M.: The relationship between Blount's disease and bow legs. Brit. J. Radiol., 41 :107-114, 1968.
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3. Blount, W. P.: Tibia vara (osteochondrosis deformans tibiae). J. Bone Joint Surg., 19:129,1937. 4. Blount, W. P.: Tibia vara-Osteochondrosis deformans tibiae: In Adams, J. P. (ed.): Current Practices of Orthopedic Surgery, Vol. III. St. Louis, C. V. Mosby Co., 1966, pp. 141-156. 5. Bohm, M.: Infantile deformities of the knee and hip. J. Bone Joint Surg., 15:574-578, 1933. 6. Cattell, H. S., Levin, S., Kopits, S., et al.: Reconstructive surgery in children with azotemic osteodystrophy. J. Bone Joint Surg., 53A:216-228, 1971. 7. Engel, G. M., and Staheli, L. T.: The natural history of torsion and other factors influencing gait in childhood. Clin. Orthop., 99:12-17, 1974. 8. Fraser, D., and Calter, R B.: The diagnosis and management of the various types of rickets. PEDIAT. CLIN. NORTH AM., 5:417-441, 1958. 9. Golding, J. S. R, and MacNeil-Smith, J. D. G.: Observations on the etiology of tibia vara. J. Bone Joint Surg., 45B:320-325, 1963. 10. Hanson, L. 1.: Physiologic genu varum. Acta Orthop. Scand., 46:221-229, 1975. 11. Howarth, B.: Knock knees. Clin. Orthop., 77:233-246, 1971. 12. Jackson, D. W., and Cozen, L.: Genu valgum as a complication of proximal tibial metaphyseal fractures in children. J. Bone Joint Surg., 53A:1571-1578, 1971. 13. Kessel, L.: Annotations on the etiology and treatment of tibia vara. J. Bone Joint Surg., 52B:93-99, 1970. 14. Langenskiiild, A.: Tibia vara. Acta Chir. Scand., 103:1-22, 1952. 15. Langenskiiild, A., and Riska, E. B.: Tibia vara (osteochondrosis deformans tibiae). J. Bone Joint Surg., 46A:1405-1420, 1964. 16. MacEwan, D. W., and Dunbar, J. S.: Radiologic study of physiologic knock knee in childhood. J. Canad. Assoc. Radiol., 9:59-63, 1958. 17. Matsen, F. H., and Staheli, L. T.: Neurovascular complications following tibial osteotomy in children. Clin. Orthop., 110:210-214, 1975. 18. Morley, A. M. M.: Knock knee in children. Brit. Med. J., 2:976-979,1957. 19. Parfitt, A. M.: Renal osteodystrophy. PEDIAT. CLIN. NORTH AM., 5:681-697,1958. 20. Salenius, P., and Vankka, E.: Development of the tibiofemoral angle in children. J. Bone Joint Surg., 57A:259-261, 1975. 21. Salter, R B., and Harris, W. R: Injuries involving the epiphyseal plate. J. Bone Joint Surg., 45A:587, 1963. 22. Schopfner, C. E., and Coin, C. G.: Genu varus and valgus in children. Radiology, 92:723732,1969. 23. Schrock, R D.: Peroneal palsy following derotation osteotomies for tibial torsion. Clin. Orthop., 62:172-177, 1969. 24. Sherman, M.: Physiologic bowing of the legs. South. Med. J., 53 :830-836,1960. 25. Smith, R: The pathophysiology and management of rickets. Orthop. Clin. North Am., 3:601-621,1972. 26. Steel, H. H., Sandrow, R E., and Sullivan, P. D.: Complications of tibial osteotomy in children for genu varum or val gum. J. Bone Joint Surg., 53A:1629-1635, 1971. 27. Stelling, F. H., and Myer, L. C.: Bow legs and knock knees in childhood. PEDIAT. CLIN. NORTH AM., 2:1053-1071,1955. 28. Taylor, S. L.: Tibial overgrowth: A cause of genu valgum. J. Bone Joint Surg., 45A:659, 1963. 29. Thelander, H. E., and Fitzhugh, M. L.: Posture habits in infancy affecting foot and leg alignments. J. Pediat., 21 :306-314, 1942
Suite 111 2850 Sixth Avenue San Diego, California 92103
Bow Legs and Knock Knees William McDade, M.D. *
Bow legs (genu varum) and knock knees (genu valgum) are common findings that affect the lower extremities of growing children. While the great majority of these problems represent normal physiologic development, and correct themselves in time without treatment, it is important for the physician to differentiate between physiologic angular deformities and those that may be pathologic, requiring special evaluation and treatment. A detailed classification of bow legs and knock knees has been set forth by Stelling and Meyer.27 The most common causes of bow legs and knock knees-physiologic varus and valgus, Blount's disease, rickets, and trauma-are discussed.
Natural History Many authors have attempted to define the natural variation and growth of the lower extremities as they relate to the position of the knee. Bohm5 was the first to suggest that bow legs and knock knees might represent normal growth patterns in infants and children. He described differences in the height and breadth of the proximal tibia and distal femoral epiphysis, suggesting that these variations were a cause for bow legs seen in infancy and knock knees recognized later in childhood. Since that time, others7, 10, 18,20,22 have examined large numbers of children both clinically and radiographically for bow leg and knock knee deformity. Their conclusions are similar and consistent with the recognition of a varoid stage of development of the knees up to the age of two years, which undergoes transition into a valgoid stage of knee development up to about age seven years. These changes are felt to represent normal physiologic development. Extremes of varus and valgus in infancy and childhood are to be expected, and may be related to or accentuated by sleeping positions, posture, ligament laxity, and torsional malalignment. Salenius,20 in the most detailed study to date, examined 1480 infants and children clinically and by x-ray, with computer analysis, using the tibiofemoral angle as a measurement point. Varus was present in in"Assistant Clinical Professor of Orthopaedic Surgery, University of California, San Diego, California Pediatric Clinics of North America- VoL 24, No.4, November 1977
825
826
WILLIAM McDADE DEVELOPMENT OF THE TIBIO-FEMORAL ANGLE DURING GROWTH VARUS VALGUS
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Figure 1. Development of the tibiofemoral angle during growth based on 1480 measurements of the tibiofemoral angle of children at different ages. (From Salenius, P.", and Vankka, E.: Development of the tibiofemoral angle in children. J. Bone Joint Surg., 57A:259-261, 1975, with permission.)
Figure 2. A, Leg alignment in this 15 month old boy appears "normal" without evidence of varus or valgus. B, Standing x-ray film of the same infant. The tibiofemoral angle approaches zero. The· epiphyses are ovoid and the transverse planes of the epiphyseal lines of the knee and ankle are relatively horizontal.
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fants less than one year of age. The knees began to straighten between the ages of one to one and a half years, and during the second and third year of life the tibiofemoral angle changed to marked valgus, which appeared to correct itself to lesser valgus in later childhood. The tibiofemoral angles were the same in boys and girls (Fig. 1).
"The Normal Infant" The normal infant usually stands with the legs somewhat apart. Infant fat may mask early physiologic varus. Standing x-rays reveal the femur and tibia to be normally aligned, without evidence of significant varus or valgus. There is no significant flaring of the distal femoral and proximal tibial metaphysis, and no asymmetrical cortical thickening of the tibial shaft. The epiphyses are oval, and the transverse planes of the epiphyseal lines are horizontal. The findings are symmetrical (Fig. 2). PHYSIOLOGIC VARUS. A mild degree of bow legs is not uncommon in children under the age of two years. Internal tibial torsion often accompanies physiologic genu varum, and its presence will accentuate the bow leg attitude in stance and with ambulation. X-rays reveal a slight lateral bow of the femur and tibia, giving rise to a varus appearance of the knee. There is flaring of the distal femoral and proximal tibial metaphysis. Thickening of the medial cortical wall of the tibia is commonly seen. The epiphysis may appear wedged medially. The transverse plane of the distal tibial epiphysis is tilted medially. The findings are symmetrical. Physiologic varus should correct by the age of two years (Fig. 3). PHYSIOLOGIC VALGUS. Physiologic knock knee is usually observed at age two and a half or three years. The x-ray appearance of the valgus knee is different, due to the older age of the child with advancing ossification of the skeletal system. The epiphyseal centers are larger, and the metaphyseal ossification has progressed to eliminate much of the metaphyseal flaring. There is no tibial cortical thickening. The planes of the epiphysis are relatively horizontal (Fig. 4). Pes planus and external tibial torsion may accompany genu valgum, and will accentuate the appearance of knock knees (Fig. 5). CLINICAL EVALUATION. Evaluation of the child with varus or valgus deformity should include a family history, leg measurements for inequality and asymmetry, observations for ligament laxity and pes planus, and observations for malalignment of the lower extremities (femoral and tibial torsion). TREATMENT. Recognizing that infants up to the age of one to one and a half years demonstrate a normal physiologic varus, and children between the ages of two and seven years demonstrate a normal physiologic valgus, treatment is not indicated. While sleeping splints, corrective shoes, and active and passive exercises have been advocated, no difference or change in the appearance of the extremities has been noted that would otherwise be expected through normal growth and development. In fact, utilization of the Denis-Browne bar to correct a physiologic genu varum is probably contraindicated, and will only "exaggerate" the physiologic knock knees that will develop later. While shoe correction in the form of wedges may improve the "tracking" with ambula-
828
WILLIAM McDADE
Figure 3. A, Twelve month old girl with physiological varus. Note wide-based stance, bow legs, and internal rotation attitude. The lateral flare or prominence of the lower leg is accentuated by the infant fat and internal tibial torsion. B, Standing x-ray. Note the medial flaring of the distal femoral and proximal tibial metaphysis, asymmetrical cortical thickening of the tibia, and the medially directed distal tibial epiphysis. The tibiofemoral angle measures 12° of varus. C, Resolution of physiologic varus at 21 months of age. Note straighter appearance of legs with less toeing in. No treatment was given. D, Standing x-ray. There is less flaring of the femoral and tibial metaphysis. The plane of the distal tibial epiphysis is less medially directed. The tibiofemoral angle measures 3° of varus.
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Figure 4. A, Three and one half year old girl with physiological valgus. B, Standing x-ray. Tibiofemoral angle measures 10 0 of valgus. C, Same girl at age eight years. Note clinical improvement in leg alignment without treatment. D, Standing x-ray. Tibiofemoral angle measures 4 0 of valgus.
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WILLIAM McDADE
Figure 5. A. Five year old boy with knock knees and outward rotation of lower legs, and flat feet. B, Examination showing clinical external tibial torsion. External tibial torsion and pes planus will accentuate the appearance of physiologic valgus. C, Standing xrays. Tibiofemoral angle measures 10 of valgus. Despite the similar tibiofemoral angle here and in Figure 4B, note how the external tibial torsion in Figure 5A accentuates the knock knee deformity as compared with Figure 4A (no external tibial torsion). 0
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tion, it will have no effect on the resolution of the normal physiologic varus or valgus. Reassurance and regular follow-up are the only specific treatment indicated for physiologic genu varum or val gum. X-rays are generally not indicated for this group.
Extreme Variation When does normal physiologic bow leg and knock knee represent an "extreme variation" that requires additional evaluation and treatment, and when is it pathologic? Bow legs that are unilateral or asymmetrical and are present beyond the age of two years, particularly in Black infants, may represent pathological conditions that require further investigation. A varus deformity that is not resolving by 18 to 24 months of age with a tibiofemoral angle of 25° or more of varus (on x-ray), especially in a Black infant, has a bad prognosis for spontaneous resolution and should be braced (Figs. 6 and 7). Knock knees in children under the age of seven may be safely ignored, unless excessive (a measured tibiofemoral angle of greater than 15° of valgus), asymmetrical, or accompanied by shortened stature. Howarth l l felt that if a knock knee deformity was excessive (greater than three inches measured between the medial malleoli) at the age of 10 years, the deformity was not likely to correct with time. He believed excessive genu valgum contributed to awkwardness of gait, subluxing patella, easy fatigability, and jOint pains. For this set of circumstances, he recommended surgical stapling of the medial distal femoral and/or medial proximal tibial epiphysis in girls at age 10 or 11 years and boys at age 12 or 13 years to correct the angular deformity. Unilateral or asymmetrical varus or valgus may be associated with tumors, congenital deformities, and trauma, while symmetrical extreme varus or valgus may be a manifestation of metabolic or endocrine disease. Blount's Disease (Tibia Vara) Blount's disease (tibia vara, osteochondrosis deformans tibiae) is a growth distrubance involving the epiphyseal-metaphyseal region of the posterior-medial aspect of the proximal tibia, resulting in a severe bow leg deformity. Significant internal tibial torsion is usually associated with the deformity. The condition was first described by Erlacher in 1922, reviewed and put into proper perspective by Blount in 1937. 3 Two stages of the deformity are recognized: an infantile form which is usually bilateral, progressive, and associated with significant internal tibial torsion; and a juvenile form recognized between the ages of 6 and 14 years which is usually unilateral. The varus deformity is milder but there may be more shortening of the involved leg. The juvenile type is much less common than the infantile type. It is impossible to distinguish between the initial stage of Blount's disease and cases of extreme physiologic genu varum, and it may be that the "extreme variation" of physiologic genu varum represents the initial stage of Blount's disease. The clinical diagnosis is usually not made until the child begins to walk. There appears to be a genetic-famil-
832
Figure 6.
WILLIAM
McDADE
A, The "extreme variation," a 15 month old boy who walked at age 10 months.
B, Internal tibial torsion is present and accentuates the bow leg appearance. C, Standing x-ray. Findings are similar to Figure 3B, but with more metaphyseal flaring, medial wedging of the epiphysis, and more pronounced varus. The tibiofemoral angle measures 25". D, Stand-
ing x-ray at age 21 months. Tibiofemoral angle measures 32" of varus. Normally the physiologic varus should be spontaneously correcting by this age. This degree of deformity represents an "extreme variation" of physiologic varus, is unlikely to improve spontaneously, and may represent the precursor of true Blount's disease. The extreme degree of varus at this age and the poor prognosis in the black infant require treatment with braces at this age. The clinical appearance at this age of extreme physiologic varus cannot be differentiated from the early stage of Blount's disease.
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A
Figure 7. Braces used for treatment of "extreme varus" and Blount's disease: long leg brace with lateral pull strap (A), A-frame brace (B), and Blount brace (C). (Courtesy of Robert Hensinger, M.D., University of Michigan.)
c ial background and geographical distribution, with most cases reported from the West Indies, West Africa, and Scandinavia. Blacks appear to be particularly affected. There is disagreement as to the etiology. LangenskiOld14 , 15 and Blount3 ,4 think the condition represents a disturbance in growth and ossification (dysplasia of bone) of the medial part of the proximal tibial epiphysis-metaphysis, whereas Golding-McNeil,9 Kessel,I3 and Bateson!' 2 believe that. the problem develops as a result of early walking patterns (particularly in Blacks) with abnormal lines of force transmitted across the medial tibiofemoral compartment. RADIOGRAPHIC FINDINGS. Langenskiold14,15 described six stages of x-ray progression (Stages I to VI) of Blount's disease (Fig. 8) based on the degree of epiphyseal depression and metaphyseal fragmentation in-
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WILLIAM McDADE II
III
IV
2-3 years
V
VI
10·13 years
Complete restoration
Restoration
common
possible
Figure 8. X-ray tracings illustrating the various stages of Blount's disease (From LangenskiOld, A.: Tibia vara. Acta Chir. Scand., 103:1-22,1952, with permission.)
volving the proximal medial tibial epiphyseal-metaphyseal junction. The earliest x-ray finding is that of an abrupt medial angulation and fragmentation at the proximal aspect of the tibia (Fig. 9). Stage I may be difficult to distinguis~from the x-ray findings of extreme physiologic genu varum. The progres'sive x-ray findings parallel the progressive clinical deformity in infantile tibia vara. X-ray findings of adolescent tibia vara reveal a lesser degree of varus deformity. The epiphyseal line medially is significantly narrowed (Fig. 10). NATURAL HISTORY OF TREATMENT. Treatment depends upon the degree of deformity (clinical and x-ray) and the age of the patient. The first four years of life are the main period of progression of Blount's disease, after which time the deformity, while continuing to progress, does so at a slower speed. Conservative treatment is recommended under the age of three years with close observation and/or appropriate bracing (see Fig. 7). If the varus deformity is not improving by age 18 months to 2 years, Stages I and II may be braced successfully. For the child who demonstrates a persistent varus with the tibiofemoral angle measuring more than 15 of varus, and Stage III or more, osteotomy is usually required. Bracing may be effective up to the age of three years; but with progressive clinical and x-ray deformity, early osteotomy is recommended (usually between the ages of four and eight years). Osteotomy done at an early age will usually completely correct the deformity permanently, with greater chances for recurrence if the osteotomy is done in later years. 0
Rickets Rickets is a disease process of the growing skeleton caused by a disturbance in calcium and phosphorus metabolism, characterized by inadequate calcification of the bone matrix. Due to the fact that the epiphyseal ends of the bone are the sites of the most active osteogenesis, the disease is most apparent here. Causes of rickets include vitamin D deficiency, renal tubular insufficiency, chronic renal insufficiency, hypophosphatasia, and vitamin D refractoriness. Vitamin D-deficient rickets
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is rarely seen in the United States. Rickets due to renal tubular insufficiency (failure of reabsorption of phosphate) includes many different forms and is becoming more commonly diagnosed. Chronic renal insuffiCiency caused by generalized kidney failure affecting both the glomeruli and tubules (renal rickets, renal osteodystrophy) has become more important with the advent of kidney transplantation and renal dialysis. Hypophosphatasia is an inborn error of metabolism characterized by low alkaline phosphatase activity. Vitamin D-refractory rickets is an inherited disorder treated by the administration of large doses of vitamin D. Figure 9.
Figure 10. Figure 9. X-ray of two year old boy with unilateral Blount's disease (stage I). Figure 10. X-ray of adolescent child with unilateral Blount's disease (stage V).
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WILLIAM McDADE
Figure 11. X-ray appearance of rickets. Note bowing of the legs, widening of the epiphyseal line, and irregularity of the metaphyseal epiphyseal junction.
The clinical picture and x-ray findings in most forms of rickets reveal an individual who may be short in stature with poor muscle tone, joint pain, and with various angular deformities affecting the weight bearing portions of the skeleton, particularly bow legs and knock knees. Genu valgum appears to be particularly common with chronic renal insufficiency, with genu varum being more common in vitamin Ddeficient rickets and vitamin D-refractory rickets. The x-ray findings are relatively similar, with osteoporosis, bowing of the long bones, widening of the epiphyseal plate, fraying of the metaphysis, and cortical thinning (Fig. 11). The diagnosis of the various forms of rickets is made by history, appropriate laboratory studies, and x-ray evaluation. TREATMENT. Recognition of the various forms of rickets and the application of specific treatment programs, plus the advent of renal transplantation and kidney dialysis, have changed the outlook for the ,.child with rickets rather abruptly over the past few years. With proper medical management, a longer life can be expected and a more aggressive approach to the angular deformities affecting these children is reasonable. Treatment of the angular deformity which was often conservative in the past due to the limited lifespan can now be more aggressive to include osteotomies when angular deformities require them. It is recommended that orthopedic care be limited to conservative treatment
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Figure 12. A, X-ray of two year old girl with undisplaced fracture of the proximal tibia. Fibula is not fractured. B, One year later the same girl exhibits pronounced unilateral valgus of previously injured leg. C, Standing x-ray shows valgus of healed tibia. Bowing occurs at the fracture site from tibial overgrowth and tethering effect of uninjured fibula. D, Correction by osteotomy of tibia and fibula. E, Clinical appearance at age five years (two years after osteotomy of tibia and fibula).
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WILLIAM McDADE
until the child is optimally controlled medically. Splints and braces may be used to control angular deformity at this age. No specific guidelines are available for the degree of deformity in rickets requiring osteotomy. Clinical judgment must include the age and maturity of the patient, degree and progression of deformity, and medical status. It is important to remember that four to six weeks prior to any operative procedure vitamin D (if being used) should be discontinued to prevent hypercalcemia and hypercalcinuria with associated kidney and central nervous system damage. Immobilization should be kept at a minimum to prevent osteoporosis. Trauma Trauma to the proximal tibia may take the form of fracture, infection, or surgery. Direct injury to the epiphyseal-metaphyseal complex (particularly the Salter IV and V injuries):!1 may lead to predictable angular deformity. It is not generally recognized that seemingly innocuous injuries of the tibia (undisplaced fractures of the proximal tibial shaft without fracture of the fibula) may lead to progressive valgus of the knee with angulation occurring at the fracture site. 12 , 28 Parents should be advised of this potential deformity (Fig. 12). It has been recognized that asymmetrical valgus may occur from such conditions as osteomyelitis involving the proximal tibia metaphysis, and from surgery performed on the proximal tibia (i.e., osteotomy of the tibia without osteotomy of the fibula). Deformities occur due to stimulation of the proximal tibial growth plate, with a tethering effect rendered by the intact fibula, and development of progressive valguS. 28 Tibial Osteotomy It is not the purpose of this paper to discuss the surgical approach or technique of tibial osteotomy for the correction of genu varum or val gum. However, recent reports l7 , 23, 26 have all documented significant complications in regard to the neurovascular status of the lower extremity in association with osteotomies done on the proximal tibia for rotational or angular deformity. It should be kept in mind that any child who undergoes a tibial osteotomy presents a potential hazard, and should be observed carefully for problems of compromise to the neurovascular or motor status of the lower extremity in the postoperative period. Other Causes of Knock Knees and Bow Legs Many other conditions may cause bow legs and knock knees in children, such as congenital anomalies, tumors, infection, paralytic deformities, metabolic/endocrine disorders, and dysplasias of bone. These conditions each require individual evaluation and treatment. REFERENCES 1. Bateson, E. M.: Non-rachitic bow leg and knock knee deformities in young Jamaican children. Brit. J. Radiol., 39:92-101, 1966. 2. Bateson, E. M.: The relationship between Blount's disease and bow legs. Brit. J. Radiol., 41 :107-114, 1968.
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3. Blount, W. P.: Tibia vara (osteochondrosis deformans tibiae). J. Bone Joint Surg., 19:129,1937. 4. Blount, W. P.: Tibia vara-Osteochondrosis deformans tibiae: In Adams, J. P. (ed.): Current Practices of Orthopedic Surgery, Vol. III. St. Louis, C. V. Mosby Co., 1966, pp. 141-156. 5. Bohm, M.: Infantile deformities of the knee and hip. J. Bone Joint Surg., 15:574-578, 1933. 6. Cattell, H. S., Levin, S., Kopits, S., et al.: Reconstructive surgery in children with azotemic osteodystrophy. J. Bone Joint Surg., 53A:216-228, 1971. 7. Engel, G. M., and Staheli, L. T.: The natural history of torsion and other factors influencing gait in childhood. Clin. Orthop., 99:12-17, 1974. 8. Fraser, D., and Calter, R B.: The diagnosis and management of the various types of rickets. PEDIAT. CLIN. NORTH AM., 5:417-441, 1958. 9. Golding, J. S. R, and MacNeil-Smith, J. D. G.: Observations on the etiology of tibia vara. J. Bone Joint Surg., 45B:320-325, 1963. 10. Hanson, L. 1.: Physiologic genu varum. Acta Orthop. Scand., 46:221-229, 1975. 11. Howarth, B.: Knock knees. Clin. Orthop., 77:233-246, 1971. 12. Jackson, D. W., and Cozen, L.: Genu valgum as a complication of proximal tibial metaphyseal fractures in children. J. Bone Joint Surg., 53A:1571-1578, 1971. 13. Kessel, L.: Annotations on the etiology and treatment of tibia vara. J. Bone Joint Surg., 52B:93-99, 1970. 14. Langenskiiild, A.: Tibia vara. Acta Chir. Scand., 103:1-22, 1952. 15. Langenskiiild, A., and Riska, E. B.: Tibia vara (osteochondrosis deformans tibiae). J. Bone Joint Surg., 46A:1405-1420, 1964. 16. MacEwan, D. W., and Dunbar, J. S.: Radiologic study of physiologic knock knee in childhood. J. Canad. Assoc. Radiol., 9:59-63, 1958. 17. Matsen, F. H., and Staheli, L. T.: Neurovascular complications following tibial osteotomy in children. Clin. Orthop., 110:210-214, 1975. 18. Morley, A. M. M.: Knock knee in children. Brit. Med. J., 2:976-979,1957. 19. Parfitt, A. M.: Renal osteodystrophy. PEDIAT. CLIN. NORTH AM., 5:681-697,1958. 20. Salenius, P., and Vankka, E.: Development of the tibiofemoral angle in children. J. Bone Joint Surg., 57A:259-261, 1975. 21. Salter, R B., and Harris, W. R: Injuries involving the epiphyseal plate. J. Bone Joint Surg., 45A:587, 1963. 22. Schopfner, C. E., and Coin, C. G.: Genu varus and valgus in children. Radiology, 92:723732,1969. 23. Schrock, R D.: Peroneal palsy following derotation osteotomies for tibial torsion. Clin. Orthop., 62:172-177, 1969. 24. Sherman, M.: Physiologic bowing of the legs. South. Med. J., 53 :830-836,1960. 25. Smith, R: The pathophysiology and management of rickets. Orthop. Clin. North Am., 3:601-621,1972. 26. Steel, H. H., Sandrow, R E., and Sullivan, P. D.: Complications of tibial osteotomy in children for genu varum or val gum. J. Bone Joint Surg., 53A:1629-1635, 1971. 27. Stelling, F. H., and Myer, L. C.: Bow legs and knock knees in childhood. PEDIAT. CLIN. NORTH AM., 2:1053-1071,1955. 28. Taylor, S. L.: Tibial overgrowth: A cause of genu valgum. J. Bone Joint Surg., 45A:659, 1963. 29. Thelander, H. E., and Fitzhugh, M. L.: Posture habits in infancy affecting foot and leg alignments. J. Pediat., 21 :306-314, 1942
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